Aryl hydrocarbon receptor nuclear translocator promotes the proliferation and invasion of clear cell renal cell carcinoma cells potentially by affecting the glycolytic pathway
- Yuxiao Zhao
- Feng Han
- Xufeng Zhang
- Chengjun Zhou
- Deqiang Huang
Affiliations: Queen Mary School, Nanchang University, Nanchang, Jiangxi 330031, P.R. China, Department of Endocrinology, The People's Hospital of Zhangqiu Area, Jinan, Shandong 250200, P.R. China, Department of Kidney Transplantation, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China, Department of Pathology, The Second Hospital of Shandong University, Jinan, Shandong 250033, P.R. China, Department of Gastroenterology, Research Institute of Digestive Diseases, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China
- Published online on: July 29, 2020 https://doi.org/10.3892/ol.2020.11917
Copyright: © Zhao
et al. This is an open access article distributed under the
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Aryl hydrocarbon receptor nuclear translocator (ARNT) is a transcription factor that has been reported to play a vital role in regulating glycolysis, angiogenesis and apoptosis. Recently, ARNT has been reported to a play role in pancreatic‑islet function in type 2 diabetes. However, the role of ARNT in kidney cancer has not yet been investigated. In the present study, ARNT expression was detected in tissues from patients with renal cell carcinoma (RCC) and in RCC cell lines. Oncomine, The Cancer Genome Atlas and cBioPortal were used to investigate the roles of ARNT in RCC. Cell migration and invasion assays were used to explore the molecular mechanisms involved. It was found that ARNT protein expression was elevated both in tissues from patients with clear cell RCC (ccRCC) and in different RCC cell lines. ARNT disruption using siRNA knockdown inhibited the migratory abilities and cell proliferation, potentially by altering the glycolysis pathway in vitro, as evidenced by decreased M2 type acetone kinase, 6‑phosphofructo‑2‑kinase/fructose‑2,6‑bisphosphatase 3 and hexokinase 2 expression. Taken together, the findings in the present study revealed a novel function of ARNT in ccRCC and indicated that ARNT promotes the proliferation and invasion of ccRCC, possibly through changes to the glycolytic pathway.